Developmental Phase-Specific Mortality After Ultraviolet-B Radiation Exposure in the Two-Spotted Spider Mite
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Published on: April 28, 2017
Yasumasa Murata1, Masahiro Osakabe1
1Laboratory of Ecological Information, Graduate School of Agriculture, Kyoto University, Japan.
Abstract:
Exposure to ambient ultraviolet-B (UVB) radiation generates DNA lesions, such as cyclobutane pyrimidine dimers and 6-4 pyrimidine-pyrimidine photoproducts in Tetranychus urticae Koch (Acari: Tetranychidae). Larvae appeared normal and healthy after UVB irradiation. Conversely, many mites were trapped in their old epidermis or experienced retarded development and shrunk, thus failing to molt from protochrysalises to protonymphs and died. This suggested that DNA lesions per se were not causing lethality in mites unless damaged genes were expressed. UVB-induced DNA lesions may have interfered with DNA replication and gene expression during the physiological changes of morphogenesis in the chrysalis stage. Comprehensive gene expression analysis by RNA sequencing revealed that gene expression involving epidermal tissue (characteristically cuticular protein genes) and myosin heavy chain muscle-like genes were downregulated in protochrysalises irradiated with UVB at the larval stage. We conclude that the success of protochrysalis molting is determined by whether the DNA lesions of genes, particularly those connected with morphogenesis, are repaired before expression at the protochrysalis stage.
Insights
Ultraviolet-B (UVB) radiation causes DNA damage in spider mites. Successful molting depends on repairing these DNA lesions before gene expression during the critical chrysalis stage.
Area of Science:
- Environmental toxicology
- Molecular biology
- Arthropod physiology
Background:
- Ambient ultraviolet-B (UVB) radiation induces DNA lesions, including cyclobutane pyrimidine dimers and 6-4 photoproducts, in terrestrial arthropods.
- Spider mites (Tetranychus urticae Koch) exposed to UVB as larvae exhibit developmental issues and mortality during the protochrysalis to protonymph molt.
- The lethality appears linked to gene expression of DNA damage rather than the lesions themselves, particularly during the physiological changes of morphogenesis.
Purpose of the Study:
- To investigate the impact of UVB-induced DNA lesions on spider mite development and survival.
- To identify the molecular mechanisms underlying UVB-induced mortality during the molting process.
- To determine the role of gene expression and DNA repair in mitigating UVB damage.
Main Methods:
- Larval exposure to ambient UVB radiation.
- Observation of mite development, molting success, and mortality.
- RNA sequencing for comprehensive gene expression analysis in irradiated protochrysalises.
- Focus on gene expression related to epidermal tissue and muscle development.
Main Results:
- UVB-irradiated larvae showed normal appearance but suffered developmental failures, including molting arrest and death.
- RNA sequencing revealed significant downregulation of cuticular protein genes and myosin heavy chain muscle-like genes in UVB-exposed protochrysalises.
- These findings suggest impaired morphogenesis due to interfered DNA replication and gene expression.
Conclusions:
- UVB-induced DNA damage can be lethal to spider mites if not repaired before gene expression during the protochrysalis stage.
- The successful molt from protochrysalis to protonymph is contingent upon the repair of DNA lesions in genes critical for morphogenesis.
- Gene expression of epidermal and muscle-related genes is particularly sensitive to unrepaired DNA damage following UVB exposure.
